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ARTICLE
IL-27 induces the production of IgG1 by human B cells
1 Inserm U454, CHU Arnaud de Villeneuve, 371 av. Doyen Gaston-Giraud, 34295 Montpellier Cedex 05, France
2 Unversité Badji-Mohktar, Annaba, Algeria
3 Department of Experimental Pharmacology and Pathology, Schering-Plough, Biopharma, Palo Alto, CA, USA
* Corresponding Author: H. Yssel,
European Cytokine Network 2006, 17(4), 281-289. https://doi.org/10.1684/ecn.2006.0045
Abstract
It has been reported that IL-27 specifically induces the production of IgG2a by mouse B cells and inhibits IL-4-induced IgG1 synthesis. Here, we show that human naïve cord blood expresses a functional IL-27 receptor, consisting of the TCCR and gp130 subunits, although at lower levels as compared to naïve and memory splenic B cells. IL-27 does not induce proliferative responses and does not increase IgG1 production by CD19+ CD27+ memory B cells. However, it induces a low, but significant production of IgG1 by naïve CD19+ CD27– IgD+ IgG– spleen and cord blood B cells, activated via CD40, whereas it has no effect on the production of the other IgG subclasses. In addition, IL-27 induces the differentiation of a population of B cells that express high levels of CD38, in association with a down-regulation of surface IgD expression, and that are surface IgG+/int , CD20low, CD27high , indicating that IL-27 promotes isotype switching and plasma cell differentiation of naive B cells. However, as compared to the effects of IL-21 and IL-10, both switch factors for human IgG1 and IgG3, those of IL-27 are modest and regulate exclusively the production of IgG1. Finally, although IL-27 has no effect on IL-4 and anti-CD40-induced C∈ germline promoter activity, it up-regulates IL-4-induced IgE production by naive B cells. These results point to a partial redundancy of switch factors regulating the production of IgG1 in humans, and furthermore indicate the existence of a common regulation of the human IgG1and murine IgG2a isotypes by IL-27.Keywords
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Copyright © 2006 The Author(s). Published by Tech Science Press.This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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